All Relations between microtubule-associated protein tau and nucleus prepositus

Publication Sentence Publish Date Extraction Date Species
Matthias Schmitz, Katharina Wulf, Sandra C Signore, Walter J Schulz-Schaeffer, Pawel Kermer, Mathias Bähr, Fred S Wouters, Saima Zafar, Inga Zer. Impact of the cellular prion protein on amyloid-β and 3PO-tau processing. Journal of Alzheimer's disease : JAD. vol 38. issue 3. 2014-07-17. PMID:24028865. we identified tau and its phosphorylated forms as potential prp-interactors and report a novel protective function of prp(c) in ad-like tau pathology. 2014-07-17 2023-08-12 mouse
Rong-Jie Chen, Wei-Wei Chang, Yu-Chun Lin, Pei-Lin Cheng, Yun-Ru Che. Alzheimer's amyloid-β oligomers rescue cellular prion protein induced tau reduction via the Fyn pathway. ACS chemical neuroscience. vol 4. issue 9. 2014-04-14. PMID:23805846. to investigate the downstream mechanism of prp(c) and aβ oligomer interaction and their possible relationships to tau, we examined tau expression in human neuroblastoma be(2)-c cells transfected with murine prp(c) and studied the effect under aβ oligomer treatment. 2014-04-14 2023-08-12 human
Rong-Jie Chen, Wei-Wei Chang, Yu-Chun Lin, Pei-Lin Cheng, Yun-Ru Che. Alzheimer's amyloid-β oligomers rescue cellular prion protein induced tau reduction via the Fyn pathway. ACS chemical neuroscience. vol 4. issue 9. 2014-04-14. PMID:23805846. by western blotting, we found that prp(c) overexpression down-regulated tau protein and aβ oligomer binding alleviated the tau reduction induced by wild type but not m128v prp(c), the high ad risk polymorphic allele in human prion gene. 2014-04-14 2023-08-12 human
Rong-Jie Chen, Wei-Wei Chang, Yu-Chun Lin, Pei-Lin Cheng, Yun-Ru Che. Alzheimer's amyloid-β oligomers rescue cellular prion protein induced tau reduction via the Fyn pathway. ACS chemical neuroscience. vol 4. issue 9. 2014-04-14. PMID:23805846. prp(c) lacking the aβ oligomer binding site was incapable of rescuing the level of tau reduction. 2014-04-14 2023-08-12 human
Rong-Jie Chen, Wei-Wei Chang, Yu-Chun Lin, Pei-Lin Cheng, Yun-Ru Che. Alzheimer's amyloid-β oligomers rescue cellular prion protein induced tau reduction via the Fyn pathway. ACS chemical neuroscience. vol 4. issue 9. 2014-04-14. PMID:23805846. quantitative rt-pcr showed the prp(c) effect was attributed to tau reduction at the transcription level. 2014-04-14 2023-08-12 human
Rong-Jie Chen, Wei-Wei Chang, Yu-Chun Lin, Pei-Lin Cheng, Yun-Ru Che. Alzheimer's amyloid-β oligomers rescue cellular prion protein induced tau reduction via the Fyn pathway. ACS chemical neuroscience. vol 4. issue 9. 2014-04-14. PMID:23805846. treatment with fyn pathway inhibitors, fyn kinase inhibitor pp2 and mek inhibitor u0126, reversed the prp(c)-induced tau reduction and aβ oligomer treatment modulated fyn kinase activity. 2014-04-14 2023-08-12 human
Rong-Jie Chen, Wei-Wei Chang, Yu-Chun Lin, Pei-Lin Cheng, Yun-Ru Che. Alzheimer's amyloid-β oligomers rescue cellular prion protein induced tau reduction via the Fyn pathway. ACS chemical neuroscience. vol 4. issue 9. 2014-04-14. PMID:23805846. overall, our results demonstrated that prp(c) down-regulated tau via the fyn pathway and the effect can be regulated by aβ oligomers. 2014-04-14 2023-08-12 human
Rong-Jie Chen, Wei-Wei Chang, Yu-Chun Lin, Pei-Lin Cheng, Yun-Ru Che. Alzheimer's amyloid-β oligomers rescue cellular prion protein induced tau reduction via the Fyn pathway. ACS chemical neuroscience. vol 4. issue 9. 2014-04-14. PMID:23805846. our study facilitated the understanding of molecular mechanisms among prp(c), tau, and aβ oligomers. 2014-04-14 2023-08-12 human
Michael P Kurnellas, Chris M Adams, Raymond A Sobel, Lawrence Steinman, Jonathan B Rothbar. Amyloid fibrils composed of hexameric peptides attenuate neuroinflammation. Science translational medicine. vol 5. issue 179. 2013-09-30. PMID:23552370. our previous work established that amyloidogenic peptides from the small heat shock protein αb crystallin (hspb5) and from amyloid β fibrils, characteristic of alzheimer's disease, were therapeutic in experimental autoimmune encephalomyelitis (eae), reflecting aspects of the pathology of ms. to understand the molecular basis for the therapeutic effect, we showed a set of amyloidogenic peptides composed of six amino acids, including those from tau, amyloid β a4, major prion protein (prp), hspb5, amylin, serum amyloid p, and insulin b chain, to be anti-inflammatory and capable of reducing serological levels of interleukin-6 and attenuating paralysis in eae. 2013-09-30 2023-08-12 Not clear
Maya Higuma, Nobuo Sanjo, Katsuya Satoh, Yusei Shiga, Kenji Sakai, Ichiro Nozaki, Tsuyoshi Hamaguchi, Yosikazu Nakamura, Tetsuyuki Kitamoto, Susumu Shirabe, Shigeo Murayama, Masahito Yamada, Jun Tateishi, Hidehiro Mizusaw. Relationships between clinicopathological features and cerebrospinal fluid biomarkers in Japanese patients with genetic prion diseases. PloS one. vol 8. issue 3. 2013-09-30. PMID:23555862. we retrospectively analyzed age at onset and disease duration; the concentrations and incidences of 14-3-3 protein, tau protein, and abnormal prion protein (prp(sc)) in the csf of 309 gprd patients with p102l, p105l, e200k, v180i, or m232r mutations; and brain pathology in 32 autopsied patients. 2013-09-30 2023-08-12 Not clear
Hansen Wang, Carl He Ren, C Geeth Gunawardana, Gerold Schmitt-Ulm. Overcoming barriers and thresholds - signaling of oligomeric Aβ through the prion protein to Fyn. Molecular neurodegeneration. vol 8. 2013-09-20. PMID:23856335. a currently popular model sees oligomeric amyloid β (oaβ) peptides bind directly to prp to emanate a signal that causes activation of the cytoplasmic tyrosine kinase fyn, an essential player in a cascade of events that ultimately leads to nmda receptor-mediated excitotoxicity and hyper-phosphorylation of tau. 2013-09-20 2023-08-12 Not clear
Khalid Iqbal, Cheng-Xin Gong, Fei Li. Hyperphosphorylation-induced tau oligomers. Frontiers in neurology. vol 4. 2013-08-22. PMID:23966973. unlike aβ and prion protein (prp) oligomers, tau oligomerization in ad and related tauopathies is hyperphosphorylation-dependent; in vitro dephosphorylation of ad p-tau with protein phosphatase 2a (pp2a) inhibits and rehyperphosphorylation of the pp2a-ad p-tau with more than one combination of tau protein kinases promotes its oligomerization. 2013-08-22 2023-08-12 Not clear
Justin M Nussbaum, Matthew E Seward, George S Bloo. Alzheimer disease: a tale of two prions. Prion. vol 7. issue 1. 2013-08-19. PMID:22965142. moreover, the propagation of toxic, misfolded aβ and tau bears a striking resemblance to the propagation of toxic, misfolded forms of the canonical prion protein, prp, and misfolded aβ has been shown to induce tau misfolding in vitro through direct, intermolecular interaction. 2013-08-19 2023-08-12 Not clear
Katell Peoc'h, Etienne Levavasseur, Emilien Delmont, Alfonso De Simone, Isabelle Laffont-Proust, Nicolas Privat, Yassmine Chebaro, Céline Chapuis, Pierre Bedoucha, Jean-Philippe Brandel, Annie Laquerriere, Jean-Louis Kemeny, Jean-Jacques Hauw, Michel Borg, Human Rezaei, Philippe Derreumaux, Jean-Louis Laplanche, Stéphane Haï. Substitutions at residue 211 in the prion protein drive a switch between CJD and GSS syndrome, a new mechanism governing inherited neurodegenerative disorders. Human molecular genetics. vol 21. issue 26. 2013-05-15. PMID:22965875. thus, subtle differences in the prp primary structure and stability are sufficient to control amyloid plaques formation and tau abnormal phosphorylation and fibrillation. 2013-05-15 2023-08-12 human
b' Megan Larson, Mathew A Sherman, Fatou Amar, Mario Nuvolone, Julie A Schneider, David A Bennett, Adriano Aguzzi, Sylvain E Lesn\\xc3\\xa. The complex PrP(c)-Fyn couples human oligomeric A\\xce\\xb2 with pathological tau changes in Alzheimer\'s disease. The Journal of neuroscience : the official journal of the Society for Neuroscience. vol 32. issue 47. 2013-02-01. PMID:23175838.' the complex prp(c)-fyn couples human oligomeric aβ with pathological tau changes in alzheimer's disease. 2013-02-01 2023-08-12 mouse
b' Megan Larson, Mathew A Sherman, Fatou Amar, Mario Nuvolone, Julie A Schneider, David A Bennett, Adriano Aguzzi, Sylvain E Lesn\\xc3\\xa. The complex PrP(c)-Fyn couples human oligomeric A\\xce\\xb2 with pathological tau changes in Alzheimer\'s disease. The Journal of neuroscience : the official journal of the Society for Neuroscience. vol 32. issue 47. 2013-02-01. PMID:23175838.' using the antibody 6d11 to prevent oligomeric aβ from binding to prp(c), we abolished fyn activation and fyn-dependent tau hyperphosphorylation induced by endogenous oligomeric aβ in vitro. 2013-02-01 2023-08-12 mouse
Eliezer Masliah, Edward Rockenstein, Chandra Inglis, Anthony Adame, Cyrus Bett, Melanie Lucero, Christina J Sigurdso. Prion infection promotes extensive accumulation of α-synuclein in aged human α-synuclein transgenic mice. Prion. vol 6. issue 2. 2013-01-03. PMID:22460692. in neurodegenerative disorders of the aging population, misfolded proteins, such as prp(sc), α-synuclein, amyloid β protein and tau, can interact resulting in enhanced aggregation, cross seeding and accelerated disease progression. 2013-01-03 2023-08-12 mouse
Garth F Hall, Brian A Patut. Is tau ready for admission to the prion club? Prion. vol 6. issue 3. 2013-01-02. PMID:22561167. in particular, we consider (1) the possibility that prionoid behavior of misprocessed tau in neurodegenerative disease may involve other aggregation-prone proteins, including prp itself, and (2) whether "prionlike" tau lesion propagation might include mechanisms other than protein-protein templating. 2013-01-02 2023-08-12 human
P Piccardo, J Cervenak, O Yakovleva, L Gregori, K Pomeroy, A Cook, F S Muhammad, T Seuberlich, L Cervenakova, D M Ashe. Squirrel monkeys (Saimiri sciureus) infected with the agent of bovine spongiform encephalopathy develop tau pathology. Journal of comparative pathology. vol 147. issue 1. 2012-10-02. PMID:22018806. constant neuropathological features included spongiform degeneration, gliosis, deposition of abnormal prion protein (prp(tse)) and many deposits of abnormally phosphorylated tau protein (p-tau) in several areas of the cerebrum and cerebellum. 2012-10-02 2023-08-12 human
Nadia Canu, Ilaria Filesi, Andrea Pristerà, Maria Teresa Ciotti, Silvia Biocc. Altered intracellular distribution of PrPC and impairment of proteasome activity in tau overexpressing cortical neurons. Journal of Alzheimer's disease : JAD. vol 27. issue 3. 2012-08-20. PMID:21841253. we have investigated the fate of normal cellular prion protein (prp(c)) in primary cortical neurons overexpressing tau protein. 2012-08-20 2023-08-12 Not clear